The purpose of this work is to elucidate basic biochemcal immunologic mechanisms mediatng the induction and suppression of experimental allergic neuritis (EAN) in monkeys, rabbits, rats and mice. Chemically, our efforts will concentrate on the role of the P2 protein as the responsible antigen of peripheral nervous system myelin in the induction of EAN and the human disease, Guillian-Barre syndrome. Numerous peptides will be derived from the P2 protein and tested for disease-inducing properties; active peptides will be synthesized. Study of EAN in rats and mice will focus on characterization of the effector cells capable of adoptive transfer of disease; the role of suppressor cells in mediating the immune response during the course of EAN; and the genetic control of EAN at the cellular level in susceptible and resistant strains. This work will rely on the newly developed Con A method for priming lymphocytes in vitro. Study of EAN in monkeys will attempt to evaluate the role of the P2 protein in induction and suppression of EAN in this species. The state of cell mediated immunity will be evaluated by study of the response of peripheral lymphocytes to the P2 protein, myelin BP, and peptides. Comparison will be made with lymphocytes derived from patients with Guillian-Barre syndrome. Should GB and EAN lymphocytes behave similarly in their immune response to the various antigens, then this work will provide a rationale to consider suppressive studies in patients with GB syndrome based on successful suppression of EAN with P2 protein or peptides.